Auer J, Berent R, Labetanig E, Eber B
Department of Internal Medicine/Division of Cardiology and Intensive Care, General Hospital Wels, Australia.
Heart Dis. 2001 Sep-Oct;3(5):297-301. doi: 10.1097/00132580-200109000-00004.
Inflammation plays a key role in the pathogenesis of atherosclerosis. In coronary artery disease (CAD), the release of different cytokines activates cellular defense. Infiltration of neutrophils and monocytes/macrophages is detected in the vessel wall in patients with CAD. Macrophages activated by interferon gamma synthesize metalloproteinases and neopterin, a pteridin derivative that has been used as an immune marker. To determine neopterin levels in patients with chronic CAD and acute coronary syndromes, the authors studied 116 subjects: 1) 25 consecutive patients (18 men, 7 women; mean age 68.5 +/- 14.3, range 40 to 86 years) with unstable angina or acute myocardial infarction (AMI); 2) 31 consecutive patients (25 men, 6 women; mean age 64 +/- 12.7, range 47 to 83 years) with signs and symptoms of clinically stable CAD; and 3) 60 consecutive healthy blood donors (38 men, 22 women; mean age 54.4 +/- 6.23, range 44 to 66 years). Neopterin levels were determined with a commercially available enzyme-linked immunosorbent assay method. In patients with unstable angina and AMI before thrombolytic therapy, neopterin levels were not significantly different from levels in patients with stable CAD (5.97 +/- 1.4 versus 7.84 +/- 3.56 nmol/L; P = 0.15). Neopterin levels in both patient groups did not significantly differ from levels in control subjects (P > 0.1). Neopterin levels in patients with unstable angina and AMI were measured four times during a 72-hour period. The lowest value was observed at baseline and differed significantly from values after 72 hours (P < 0.001; 5.97 +/- 1.4 versus 9.25 +/- 2.36). Neopterin levels after 72 hours were also significantly different from initial values in patients with stable CAD (P < 0.001). There was no correlation between neopterin and creatine kinase (CK) levels, CK-MB isoenzyme, or troponin I as markers for the extent of the myocardial injury during the observation period. These data do not support previous reports of higher baseline levels of serum neopterin in patients with unstable angina or AMI compared with patients with chronic, stable CAD and healthy controls. Neopterin as a marker of macrophage activation is significantly increased in patients with AMI and unstable angina shortly after the onset of symptoms (after a period of 72 hours), supporting the hypothesis of monocyte and macrophage activation in patients with an acute coronary syndrome or AMI.
炎症在动脉粥样硬化的发病机制中起关键作用。在冠状动脉疾病（CAD）中，不同细胞因子的释放激活细胞防御。在CAD患者的血管壁中可检测到中性粒细胞和单核细胞/巨噬细胞的浸润。由γ干扰素激活的巨噬细胞合成金属蛋白酶和新蝶呤，新蝶呤是一种蝶啶衍生物，已被用作免疫标志物。为了测定慢性CAD患者和急性冠状动脉综合征患者的新蝶呤水平，作者研究了116名受试者：1）25例连续的不稳定型心绞痛或急性心肌梗死（AMI）患者（18名男性，7名女性；平均年龄68.5±14.3岁，范围40至86岁）；2）31例连续的有临床稳定CAD体征和症状的患者（25名男性，6名女性；平均年龄64±12.7岁，范围47至83岁）；3）60例连续的健康献血者（38名男性，22名女性；平均年龄54.4±6.23岁，范围44至66岁）。用市售的酶联免疫吸附测定法测定新蝶呤水平。在溶栓治疗前的不稳定型心绞痛和AMI患者中，新蝶呤水平与稳定CAD患者的水平无显著差异（5.97±1.4对7.84±3.56 nmol/L；P = 0.15）。两个患者组中的新蝶呤水平与对照组的水平无显著差异（P>0.1）。在72小时内对不稳定型心绞痛和AMI患者的新蝶呤水平进行了4次测量。最低值在基线时观察到，与72小时后的数值有显著差异（P<0.001；5.97±1.4对9.25±2.36）。72小时后的新蝶呤水平与稳定CAD患者的初始值也有显著差异（P<0.001）。在观察期内，新蝶呤与作为心肌损伤程度标志物的肌酸激酶（CK）水平、CK-MB同工酶或肌钙蛋白I之间无相关性。这些数据不支持先前关于不稳定型心绞痛或AMI患者血清新蝶呤基线水平高于慢性稳定CAD患者和健康对照者的报道。新蝶呤作为巨噬细胞激活的标志物在AMI和不稳定型心绞痛患者症状发作后不久（72小时后）显著升高，支持急性冠状动脉综合征或AMI患者中单核细胞和巨噬细胞激活的假说。
